Week 10 - Ischaemic Heart Disease Flashcards
What are the risk factors for coronary atheroma?
Non-modifiable: - Increasing age - Male gender (females catch up after menopause) - Family history Modifiable: - Hyperlipidaemia - Cigarette smoking - Hypertension - Diabetes mellitus - Exercise, obesity, stress (less important)
What are the differences between a stable and vulnerable plaque?
- Stable: small necrotic centre, thick fibrous cap, cap less likely to fissure/rupture
- Vulnerable: large necrotic centre, thin fibrous cap, cap more likely to fissure/rupture
What is ischaemic chest pain?
Any IHD can cause chest pain that is central, retrosternal or left-side
- Pain may also radiate to the shoulders and arms, along with the neck, jaw, epigastrium and back (can present here without chest pain)
- Pain = tightening, heavy, crushing, constricting
- Pain varies in intensity and duration
- Pain onset, precipitating, aggravating and relieving factors and associated symptoms all vary
- Gets progressively worse from stable angina, to unstable angina, to MI
What is stable angina?
- Atheromatous plaques build up in the coronary vessels
- – The plaques have a necrotic centre and fibrous cap
- – Occlude more and more of the lumen, leading to ischaemia of the myocardium
- Angina occurs when the plaque occludes >70% of lumen
- Flow is sufficient at rest, so pain is relieved when demand stops
- Transient ischaemia during periods of increased O2 demand
- May progress gradually over time
- Mild-moderate pain
- No myocyte injury or necrosis
How can you treat stable angina?
- Acute episodes: sublingual nitrate spray/tablet (venodilates, deduces preload)
- Prevent episodes: ß-blocker (decrease heart rate and contractility), Ca2+ channel blockers (decrease after load by peripheral vasodilation)
- Oral nitrates
- Prevent cardiac events: aspirin (decreased platelet aggregation so decreased thrombus formation if plaque is disrupted), statins (decrease LDL cholesterol, decrease progression of atherosclerosis, increase plaque stability)
- Long term: consider revasculatisation (mechanically restores blood flow using coronary angioplasty and stenting)
How do you investigate stable angina?
Clinical diagnosis:
- Based on history
- No specific signs on examination
- May have risk factors (high BP, corneal arcus)
- Signs of atheroma elsewhere
Resting ECG:
- Usually normal
- May show signs of previous MI
Exercise stress test to confirm diagnosis:
- Graded exercise on a treadmill connected to an ECG until either:
— Target heart rate is reached
— Chest pain occurs
— ECG changes
— Other problems (e.g. Arrhythmia)
- Test is positive if ECG shows ST depressions of >1mm
What is unstable angina?
As angina worsens due to the profession of the formation of the atheromatous plaque, it progresses from stable to unstable angina
- Due to increased lumen occlusion
- Classified as Ischaemic chest pain that occurs at rest
- Severe pain
- Occurs with a crescendo pattern
What is acute coronary syndrome?
Sudden plaque fissuring with thrombus formation
- Relates to a group of symptoms attributed to the obstruction of the coronary arteries
- If occlusion is complete and persistent, and a large area of myocardium without collateral circulation is affected, it will result in STEMI
- If there is a non-occlusive thrombus, brief occlusion, collaterals present and a small area of myocardium is affected, then is results in NSTEMI or unstable angina
What is a myocardial infarction?
- A complete occlusion of a coronary vessel, leading to an infarct of the myocardium it supplies
- The fibrous cap of the atheromatous plaque can undergo erosion or fissuring, exposing blood to the thrombogrnic material in the necrotic core
- The platelet ‘clot’ is followed by a fibrin thrombus which can either occludes even entire vessel where it forms or break off to form an embolism
- Typically presents with ischaemic chest pain
- Pain is very severe, persistent pm at rest, often has no precipitate
- Pain is not relieved by rest or nitrate spray
- Patient may be breathless, faint, sweating, nauseous, vomiting and have pallor
What is NSTEMI?
Non ST elevated MI
- Infarct is not full thickness of the myocardium
- ST depression
- Partial/brief occlusion or adequate collateral circulation
- Injury limited to more vulnerable sub-endocardial areas
What is STEMI?
ST elevated MI
- Infarct is full thickness of myocardium
- Most have total occlusion of an artery
- Injury extends to dub epicardial side
What are the signs/symptoms of MI?
- Patient is anxious/distressed
- Sweating, pallor
- Cold, clammy skin
- Tachycardia/arrhythmias
- Low BP
- Signs of heart failure
What are the ECG changes during a STEMI?
- Hyperacute T wave
- ST elevation
- Q wave
- ST-elevation with T wave inversion
- T wave recovery
How can you identify a previous MI on an ECG?
Via the persistence of the pathological, deepened Q wave
What are the principles of management of angina, acute MI and unstable angina?
- Prevent thrombosis (anti-platelet drugs, anticoagulants)
- Dissolve thrombus (fibrinolytic agents)
